Toxicity, Ciguatera
Author: Thomas Arnold, MD, Medical Director, Louisiana Poison Control Center, Associate Professor and Chairman, Department of Emergency Medicine, Section of Clinical Toxicology, Louisiana State University Health Sciences Center
Contributor Information and Disclosures
Ciguatera poisoning is the most common nonbacterial, fish-borne poisoning in the United States. It is caused by consumption of reef fish that feed on certain dinoflagellates (ie, algae) associated with coral reef systems. At least 5 types of ciguatoxin have been identified and are noted to accumulate in larger and older fish higher up the food chain. Ciguatera poisoning has been a significant concern in tropical areas for centuries and generally is believed to be confined to coral reef fish in water between the latitudes of 35 degrees north and 35 degrees south. In the modern era of world travel and rapid transportation, many warm-water fish are available commercially in markets throughout the world, and cases of ciguatera poisoning may be seen in any location.
For related fish-borne poisoning articles, see Toxicity, Scombroid, Toxicity, Shellfish, and Toxicity, Seafood.
Pathophysiology
Gambierdiscus toxicus is the dinoflagellate most notably responsible for production of ciguatoxin, although other species have been identified more recently. More than 400 species of fish have been implicated in ciguatera poisoning, starting with herbivores and then climbing up the food chain to the larger carnivorous fish.
Species of fish most frequently implicated include groupers, amberjack, red snappers, eel, sea bass, barracuda, and Spanish mackerel. Fish larger than 2 kg contain significant amounts of toxin and readily produce toxic effects when ingested. Although not completely reliable, an immunoassay and a mouse biologic assay are available for detection of ciguatoxin in affected fish. Ciguatoxin and other similar toxins are heat stable and lipid soluble; they are unaffected by temperature, gastric acid, or cooking method. Presence of toxin does not affect odor, color, or taste of the fish. Recently, chemists have been successful in synthesizing specific ciguatoxins, ensuring a practical supply will be available for future biological applications.
Ciguatoxin produces toxic effects by activation of voltage-dependent sodium channels, resulting in hyperexcitability, decreased conduction, and prolonged refractoriness. Effects are most pronounced on neuronal, cardiac, and GI tissues.
Frequency
United States
Most ciguatera outbreaks in the United States occur in Hawaii and Florida, although tourists may develop symptoms after returning home. Global marketing of tropical fish has been responsible for sporadic cases reported across the United States mainland.
According to the 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS), 175 single exposures to ciguatera were reported.1
International
Annually, an estimated 50,000 cases of ciguatera poisoning occur worldwide;2,3 however, this poisoning is difficult to track and is thought to be underreported. Ciguatera poisoning is endemic in Australia, the Caribbean, and the South Pacific islands. No doubt exists that ciguatera has had a substantial economic impact on many of the Third World countries where it is endemic.
Mortality/Morbidity
Ciguatera poisoning seldom is lethal. Typical mortality rate is 0.1%, although rates as high as 20% have been reported. Death usually is attributed to cardiovascular depression, respiratory paralysis, or hypovolemic shock.
The 2007 Annual Report of the American Association of Poison Control Centers' NPDS reported 32 minor outcomes, 48 moderate outcomes, 4 major outcomes and no deaths.1
Race
Several reports note that patients of similar ethnic backgrounds tend to share common symptom groupings.
Age
Children appear to be affected more severely and are involved more often in life-threatening cases.
Clinical
History
Currently, ciguatera poisoning is a clinical diagnosis based upon a constellation of symptoms temporally related to ingestion of suspect fish products. Onset of symptoms may be within 15 minutes or as late as 24 hours (rarely) after ingestion of the toxin. Generally, symptoms are noted within 6-12 hours after ingestion of tropical reef fish. Symptoms increase in frequency and severity over the subsequent 4-6 hours. Reported symptoms are numerous but commonly affect 3 major organ systems: GI, neurologic, and cardiovascular.
•GI symptoms often are the first to appear, may last 1-2 days, and include the following:
◦Abdominal pain
◦Nausea
◦Vomiting
◦Diarrhea
•Neurologic symptoms usually are multiple, varied, and, at times, bizarre. Symptoms may begin within a few hours to 3 days after the meal and can be persistent, lasting weeks to several months. Symptoms may include the following:
◦Lingual and circumoral paresthesias
◦Painful paresthesias of the extremities
◦Paradoxical temperature reversal (eg, cold objects feel hot and hot objects feel cold) (This is a classic reported finding; however, at least one study suggests that this perception is likely the result of the exaggerated and intense nerve depolarization and that gross temperature perception remains intact).
◦Dental pain (teeth feel loose)
◦Pruritus
◦Arthralgias
◦Myalgias
◦Weakness
◦Ataxia, vertigo
◦Respiratory paralysis
◦Coma
•Cardiovascular symptoms are less common but can be severe. They usually resolve within 2-5 days. Patients may experience weakness and dizziness from bradycardia and hypotension.
•Other features include dyspnea, sweating, salivation, chills, neck stiffness, and pruritus.
Physical
•Dehydration from GI losses is a common finding.
•Neurologic findings are extremely variable, from mild to life threatening.
•Cardiovascular findings include bradycardia and hypotension. Signs of shock may be observed. Hypotension results from the following:
◦Fluid loss
◦Bradycardia
◦Peripheral vasodilation
◦Myocardial depression
Causes
Ingestion of sufficient quantities of fish with accumulated ciguatoxin produces this syndrome.
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